Page 854 - Adams and Stashak's Lameness in Horses, 7th Edition

820 Chapter 7

BONE INJURIES AND DISEASE

VetBooks.ir ChrIs KaWCaK and Gary M. Baxter

THE IMMATURE SKELETON horses. (The reader is referred to Chapter 10 for further
information on physeal fractures in horses.) Non‐frac­
Bone growth occurs by both longitudinal (endo­ ture injuries are not uncommon in foals. Chronic angu­
chondral) and circumferential (membranous) growth. lar limb deformity (ALD) and the resultant overstress of
Membranous bone formation is responsible for increases both local and distant physes in the limb can result in
in long bone width and formation of flat bones and is growth abnormalities and permanent deformity. More
independent of a cartilaginous template. Longitudinal subtle, chronic stresses to the physes, as is common in
bone growth results from a series of events occurring at juvenile human athletes, are not recognized in horses.
highly specialized regions at one or both ends of the However, the size and rapid growth of horses seem to
bone. These regions are referred to as the physes, growth make them predisposed to such problems.
plates, or, more correctly, the metaphyseal growth
plates. The process that occurs at the growth plate,
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termed endochondral ossification, is characterized by Developmental Orthopedic Diseases
rapidly differentiating and maturing cartilage cells and Developmental orthopedic disease (DOD) complex is
the replacement of cartilage by bone. There are two a group of abnormalities that occurs in foals and young
types of growth plates: discoid and spherical. The dis­ growing horses. Other terms that are often used inter­
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coid growth plates are seen at the ends of long bones. changeably with DOD include osteodystrophy or osteo­
Some bones have a physis at each end of the bone, chondrosis although this is considered erroneous. Most
whereas others, such as the third metacarpal/metatarsal of the diseases included in the DOD complex can be
bone and the proximal and middle phalanges, have only attributed to alterations in bone growth or development
one distinguishable physis. A discoid physis is located (endochondral ossification) either at the metaphyseal or
between the metaphysis (the flared end of the bone that epiphyseal growth plates. These include physitis, ALDs,
contains spongy bone) and the epiphysis. An apophysis OCD, subchondral cystic lesions (SCLs), cuboidal bone
(which is a type of discoid physis) is an epiphysis that is collapse or incomplete ossification, juvenile arthritis,
subject to tensile rather than compressive forces, such as cervical vertebral malformations (CVM), and flexural
at the olecranon process, calcaneal tuber, and tibial deformities. 48,131 The more specific term “juvenile osteo­
tuberosity. The growth plate of an apophysis contains chondral conditions” has been proposed to describe
greater amounts of fibrocartilage than a true discoid those DOD lesions specific to the immature joint and
physis, which is an adaptation to withstand tensile growth plate. These include osteochondrosis/OCD,
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forces. Spherical physes are also located in the small cuboidal bone disease, bone cysts, osteochondral col­
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cuboidal bones of the foal’s carpus and tarsus. These lapse, insertion site avulsions, and physitis. Clinical signs
growth plates develop into bones by centrifugal expan­ of these conditions are variable but are usually seen in
sion around a central cartilage core. They begin to ossify young horses since this is an abnormality of developing
in the center and gradually assume the contours of the bone. Signs include variable degrees of lameness, altera­
bone of an adult as bone development reaches the mar­ tion in posture or positioning of the limb, crooked legs,
gins of the cartilage model. (The reader is referred to joint effusion, limb enlargement, ataxia (CVM only),
Chapter 10 for further information on the morphology and possible fractures. Additionally, multiple DOD con­
and physiology of the physis.) ditions may be present in the same animal.
Although the exact cause for DOD is not known, the
Effect of Trauma on the Physis basic pathologic mechanism of disturbed endochondral
ossification has been agreed upon, and there are multi­
When an excessive force is applied to a joint and its ple risk factors that appear to predispose young horses
nearby physis, an epiphyseal or physeal injury is likely to the development of these diseases. Despite the lack of
to occur. Similar to other injuries in adults, chronic identification of single factors that cause DOD, a pri­
repetitive trauma, such as occurs in young human ath­ mary pathologic mechanism of vascular insult has been
letes, can also result in damage to the physis. This is widely accepted. Damage to the vasculature as it
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because the cartilaginous growth plate is weaker than courses through the cartilage canals has been seen in
the surrounding bone, ligamentous structures, and joint foals, but in many cases a reparative cascade of events is
capsule. Physeal and epiphyseal injuries account for often present, leading to a mix of clinical outcomes from
approximately 15%–18% of all fractures in children clinical disease to healing. 87
and also occur commonly in foals. Injuries that would Despite the apparent common pathogenetic mecha­
normally produce a ruptured ligament or joint disloca­ nism of vascular insult, the etiologic factors that incite
tion in an adult may produce traumatic separation of disease are diverse. Many of the risk factors are man‐
the physis in a young animal. For example, trauma to made such as management and breeding practices, and
the fetlock region usually causes fetlock luxations in others have been extrapolated from research work in
adult horses and distal metacarpal/metatarsal physeal other species. 27,39,86 For instance, the incidence of devel­
fractures in foals. Joint luxations are rare in young opmental problems in wild horses is low compared with